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Moreover, upregulated expression of Lox family promoted the cross-linking of ECM components, suggesting the increased ECM stiffness (Fig
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Conversely, BACH1 knockdown not only inhibited BPC157-induced HUVEC proliferation and tube formation but also blocked the expression of these proangiogenic factors, confirming that BACH1 is the pivotal downstream effector of the BPC157-FBXO22 axis
